Resistance exercise mediates remote ischemic preconditioning by limiting cardiac eNOS uncoupling.

Area of Science:

• Cardiovascular Physiology
• Exercise Science
• Molecular Cardiology

Background:

• Long-term aerobic training provides cardioprotection via remote ischemic preconditioning (RIPC).
• RIPC triggered by acute exercise, particularly resistance exercise (RE), is poorly understood.
• Investigating RE's potential to induce cardiac RIPC via nitric oxide synthase (NOS) mechanisms.

Purpose of the Study:

• To determine if resistance exercise (RE) induces cardiac remote ischemic preconditioning (RIPC).
• To elucidate the role of nitric oxide synthase (NOS) in RE-mediated cardioprotection.
• To assess the impact of RE on myocardial ischemia-reperfusion (IR) injury.

Main Methods:

• Acute RE at 40% maximal load in rats to measure systemic nitrite and cardiac eNOS/nNOS activity.
• Induction of myocardial infarction (MI) via ischemia-reperfusion (IR) in exercised and non-exercised rats.
• Assessment of cardiac contractility, MI size, ST-segment, arrhythmias, reactive oxygen species (ROS), and protein carbonylation.

Main Results:

• RE increased systemic nitrite and cardiac eNOS phosphorylation, without affecting nNOS.
• RE fully prevented loss of cardiac contractility and reduced MI size, aberrant ST-segment, and arrhythmias.
• NOS inhibition abolished RE-mediated cardioprotection; RE prevented ROS generation and protein carbonylation by limiting eNOS uncoupling.

Conclusions:

• Resistance exercise (RE) mediates cardiac remote ischemic preconditioning (RIPC).
• RE mitigates myocardial ischemia-reperfusion (IR) injury by limiting endothelial nitric oxide synthase (eNOS) uncoupling.
• The findings highlight RE as a potential non-pharmacological intervention for cardiac protection.